Even if the molecular mechanisms of hepcidin regulation by iron, oxygen and anemia are still unclear, it is known that Interleukin 6 (IL-6) induces transcription of the hepcidin gene in hepatocytes. In inflammatory and infection disorders, cytokine induced hepcidin excess, through ferroportin binding, contributes to development of anemia of inflammation, characterized by ID and IDA despite adequate iron stores. When iron export is hindered, iron is stored in host cells. However, inflammation may contribute to ID and IDA by hepcidin-independent mechanism(s) as the down-regulation of ferroportin. Independently on hepcidin synthesis, high levels of serum IL-6 seem to down-regulate ferroportin mRNA expression, thus sequestering iron inside cells and blocking iron flow into plasma. The inability to export iron leads to hypoferremia, decreased pool of serum transferrin-Fe(III) and iron-limited erythropoiesis.